The present invention, in some embodiments thereof, relates to a method of treating patients and, more particularly, but not exclusively, to a method of treating patients according to triglyceride levels.
Flesler et al. in U.S. Pat. No. 7,512,442 disclose:
“Apparatus is provided for treating a condition such as obesity. The apparatus includes a set of one or more electrodes, which are adapted to be applied to one or more respective sites in a vicinity of a body of a stomach of a patient. A control unit is adapted to drive the electrode set to apply to the body of the stomach a signal, configured such that application thereof increases a level of contraction of muscle tissue of the body of the stomach, and decreases a cross sectional area of a portion of the body of the stomach for a substantially continuous period greater than about 3 seconds”
Ben-Haim et al. in U.S. Pat. No. 6,571,127 disclose:
“The invention comprises methods of increasing contractile force and/or the motility of a GI tract. A first method comprises selecting a portion of the GI tract and applying a non-excitatory electric field to the portion, which field increases the force of contraction at the portion.”
Lam T K et al. Hypothalamic sensing of circulating fatty acids is required for glucose homeostasis. Nature Medicine 3:320-327, 2005 disclose: “Here we postulate that physiological increments in plasma fatty acids can be sensed within the hypothalamus and that this sensing is required to balance their direct stimulatory action on hepatic gluconeogenesis.”
Leitao CB et al. Lipotoxicity and decreased islet graft survival. Diabetes Care 33; 658-660, 2010 disclose: “Higher baseline triglycerides are associated with earlier decline in islet graft function.”
PCT/IL2011/000116 filed on Feb. 1, 2011 discloses: “Apparatus (18) for treating a human patient, which includes one or more electrode contact surfaces (100), which are configured to be applied to a fundus (22) of the patient. A control unit (90) is configured to drive the one or more electrode contact surfaces (100) to apply an electrical signal to the fundus (22) that chronically improves a blood glucose level of the patient, in order to treat the patient, without calculating an impedance of tissue of the fundus (22) based on a sensed parameter that varies in response to the electrical signal, for detecting eating by the patient or a characteristic of food eaten by the patient.”
Additional background art includes:    U.S. Pat. No. 7,840,269    US patent application 2009/0281449    Matthews et al. (1985) “Homeostasis model assessment: insulin resistance and B-cell function from fasting plasma glucose and insulin concentrations in man.” Diabetologia 28: 412-9.    Pocia A et al. Cell Metabolism 1: 53-61, 2005    Schwartz MW et al. Nature 404: 661-671, 2000
The following two publications by the inventor and others should not be considered prior art, however they may assist in putting other references in context:
“Fasting plasma triglicerides predict the glycaemic response to treatments of type 2 diabetes by gastric electrical stimulation. A novel Lipotoxicity paradigm”, by HE Lebovitz et al, Diabetic Medicine. 30, 687-693 (2013), DOI: 10.1111/dme.12132.
A poster titled “21-LB Existance of a Trigliceride-dependent Glycemic Regulatory Pathway in Patients with Type 2 Diabetes”, by HE Lebovitz et al. and presented at the diabetes association annual meeting Jun. 23, 2013 in Chicago
Further additional background art includes:    1 Rubino F, Schauer P R, Kaplan L M, Cummings D E. Metabolic surgery to treat type 2 diabetes: clinical outcomes and mechanisms of action. Annu Rev Med 2010; 61: 393-411.    2 Sanmiguel C P, Conklin J L, Cunneen S A, Barnett P, Phillips E H, Kipnes M et al. Gastric electrical stimulation with the TANTALUS_system in obese type 2 diabetic patients: effect on weight and glycemic control. J Diabetes Sci Technol 2009; 3: 964-970.    3 Rodriguez L, Reyes E, Fagalde P, Oltra M S, Saba J, Aylwin C G et al. Pilot clinical study of an endoscopic, removable duodenal-jejunal bypass liner for the treatment of type 2 diabetes. Diabetes Technol Therap 2009; 11: 725-732.    4 Laferrere B, Teixeira J, McGinty J, Tran H, Egger J R, Colarusso A et al. Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with Type 2 diabetes. J Clin Endocrinol Metab 2008; 93: 2479-2485.    5 Harvey E J, Arroyo K, Korner J, Inabnet W B. Hormone changes affecting energy homeostasis after metabolic surgery. Mt Sinai J Med 2010; 77: 446-465.    6 Thaler J P, Cummings D E. Food alert. Nature 2008; 452: 941-942.7 Greenway F, Zheng J. Electrical stimulation as treatment for obesity and diabetes. J Diabetes Sci Technol 2007; 1: 251-259.    8 Policker S, Haddad W, Yaniv I. Treatmentof type 2 diabetes using meal-triggered gastric electrical stimulation. Isr Med Assoc J 2009; 11: 206-208.    9 Bohdjalian A, Ludvik B, Guerci B, Bresler L, Renard E, Nocca D et al. Improvement in glycemic control by gastric electrical stimulation (TANTALUS™) in overweight subjects with type 2 diabetes. Surg Endosc 2009; 23: 1955-1960.    10 Wallace T M, Levy J C, Matthews D E. Use and abuse of HOMA modeling. Diabetes Care 2004; 27: 1487-1495.    11 Jackson S L. Research Methods and Statistics: A Critical Thinking Approach. 4th edition. Belmont, C A: Publisher Wadsworth, 2011.    12 Ravikumar B, Gerrard J, Man C D, Firbank M J, Lane A, English P T et al. Pioglitazone decreases fasting and postprandial endogenous glucose production in proportion to decrease in hepatic triglyceride content. Diabetes 2008; 57: 2288-2295.    13 Korenblat K M, Fabbrini E, Mohammed B S, Klein S. Liver, muscle, and adipose tissue insulin action is directly related to intrahepatic triglyceride contentin obese subjects. Gastroenterology 2008; 134: 1369-1375.    14 Unger R H, Scherer P E. Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity. Trends Endocrinol Metab 2010; 21: 345-352.    15 Del Prato S. Role of glucotoxicity and lipotoxicity in the pathophysiology of Type 2 diabetes mellitus and emerging treatment strategies. Diabet Med 2009; 26: 1185-1192.    16 Adams J M II, Pratipanawatr T, Berria R, Wang E, DeFronzo R A, Sullards M C et al. Ceramide content is increased in skeletal muscle from obese insulin-resistant humans. Diabetes 2004; 53: 25-31.    17 Morino K, Petersen K F, Shulman G I. Molecular mechanisms of insulin resistance in humans and their potential links with mitochondrial dysfunction. Diabetes 2006; 55: S9-S15.    18 Consitt L A, Bell J A, Houmard J A. Intramuscular lipid metabolism, insulin action, and obesity. IUBMB Life 2009; 61: 47-55.    19 Gallagher E J, LeRoith D, Karnieli E. Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai j Med 2010; 77: 511-523.    20 Van Raalte D H, van der Zijl N J, Diamant M. Pancreatic steatosis in humans: cause or marker of lipotoxicity. Curr Opin Clin Nutr Metab Care 2010; 13: 478-485.    21 Lupi R, Dotta F, Marselli L, Del Guerra S, Masini M, Santangelo C et al. Prolonged exposure to free fatty acids has cytostatic and proapoptotic effect on human pancreatic islets. Diabetes 2002; 51: 1437-1442.    22 Magnan C, Cruciani C, Clement L, Adnot P, Vincent M, Kergoat M et al. Glucose-induced insulin hypersecretion in lipid infused healthy subjects is associated with a decrease in plasma norepi-nephrine concentration and urinary excretion. J Clin Endocrinol Metab 2001; 86: 4901-4907.    23 Carpentier A, Mittleman S D, Bergman R N, Giacca A, Lewis G F. Prolonged elevation of plasma free fatty acids impairs pancreatic bcell function in obese nondiabetic humans but not in individuals with type 2 diabetes. Diabetes 2000; 49: 399-408.    24 Kashyap S, Belfort R, Gastaldelli A, Pratipanawatr T, Berria R, Pratipanawatr W et al. A sustained increase in plasma free fatty acids impairs insulin secretion in nondiabetic subjects genetically predisposed to develop type 2 diabetes. Diabetes 2003; 52: 2461-2474.    25 Wang PYT, Caspi L, Lam CKL, Chari M, Li X, Light P E et al. Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production. Nature 2008; 452: 1012-1016.    26 Pocai A, Obici S, Schwartz G J, Rossetti L. A brain-liver circuit regulates glucose homeostasis. Cell Metab 2005; 1: 53-61.    27 Pocai A, Lam T K T, Gutierrez-Juarez R, Obici S, Schwartz G J, Bryan J et al. Hypothalamic KATP channels control hepatic glucose production. Nature 2005; 434: 1028-1031.    28 Leitao C B, Bernetti K, Tharavanij T, Cure P, Lauriola V, Berggren P-O et al. Lipotoxicity and decreased islet graft survival. Diabetes Care 2010; 33: 658-660.